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Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
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Regulation of the Unfolded Protein Response01:31

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

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Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
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Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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The Unfolded Protein Response01:37

The Unfolded Protein Response

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The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
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Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

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Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
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Related Experiment Video

Updated: Nov 11, 2025

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
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Ghrelin Inhibits Intestinal Epithelial Cell Apoptosis Through the Unfolded Protein Response Pathway in Ulcerative

Lin Zhang1,2, Jian Cheng1, Jie Shen2

  • 1Department of Gastroenterology, Jinshan Hospital, Fudan University, Shanghai, China.

Frontiers in Pharmacology
|March 29, 2021
PubMed
Summary

Ghrelin protects intestinal epithelial cells from apoptosis in ulcerative colitis (UC) by regulating the unfolded protein response (UPR) pathway. This finding offers potential therapeutic insights for inflammatory bowel disease (IBD).

Keywords:
apoptosisghrelinintestinal epithelial cellulcerative colitisunfolded protein response pathway

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An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Molecular Medicine

Background:

  • Ulcerative colitis (UC), a form of inflammatory bowel disease (IBD), is characterized by intestinal epithelial cell (IEC) apoptosis.
  • Ghrelin levels are decreased in IEC apoptosis induced by tumor necrosis factor-alpha (TNF-α), suggesting a potential antiapoptotic role.

Purpose of the Study:

  • To investigate the antiapoptotic role of ghrelin in ulcerative colitis (UC) progression.
  • To explore the underlying mechanisms involving the unfolded protein response (UPR) pathway.

Main Methods:

  • Utilized an in vitro TNF-α-treated Caco-2 cell model.
  • Employed in vivo mouse colitis models induced by dextran sulfate sodium (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS).
  • Assessed ghrelin's effects on apoptosis, the ghrelin receptor GHS-R1a, and the UPR pathway.

Main Results:

  • Ghrelin inhibited TNF-α-induced apoptosis in Caco-2 cells, an effect blocked by the GHS-R1a antagonist [D-lys3]-GHRP-6.
  • Ghrelin demonstrated protective effects against apoptosis in DSS- and TNBS-induced mouse colitis models, dependent on GHS-R1a.
  • Ghrelin modulated the UPR pathway and regulated key apoptosis-related proteins (caspase-3, BAX, Bcl-2).

Conclusions:

  • Ghrelin plays a significant antiapoptotic role in intestinal epithelial cells during colitis.
  • Ghrelin exerts its protective effects by modulating the UPR pathway.
  • Ghrelin represents a potential therapeutic target for managing apoptosis in UC and other IBDs.